Depression affects millions of Americans every day. Yet, depression is not a new phenomena. It has afflicted people since the beginning of recorded time. Descriptions of what we now call depression can be found in numerous ancient documents. The Old Testament, in the book of Kings, recounts the story of King Saul during a profound state of depression. In the Iliad, Homer tells of Ajax, whose depression led to his suicide. Around 400 B.C. Hippocrates began to use the term “melancholia” to describe disturbances in mood.

Nutritional Deficiencies Which Can Cause Depression
How Birth Control Pills Cause Depression
Descriptions Of How Current Anti-Depressants Can Cause Bizarre Behavior
Eat, Drink And Be Healthy Nutrition Recommendations

It is important to note that depression is not just sadness. Sadness is a feeling which is usually related to a specific event, such as a personal loss. Depression is an emotional state, which dominates one’s outlook on life. Transient feelings of depression are completely normal. Everyone feels depressed once in a while. It has been said that if it were not for episodic times of depressed moods, happy times would lose their value. But sufferers of depression do not have a transient depressed mood. These people are down every day; day after day; week after week as time goes on. Some sufferers of this disorder are able to function through daily life in spite of feelings of anxiety, insecurity and shame. These people are able to make it through the day, but are never really happy. Others are completely paralyzed in life, unable to function, sleeping throughout the day, unable to sleep at night. It is estimated that 25% of the American population suffers from depression or other alterations of mood at some time during their lifetime. Considering that one of the symptoms of depression is overeating, and understanding that fully 33% of Americans are clinically obese, it is likely that actual numbers are much bigger.

As the biochemistry of mood and behavior have become better understood, many conditions once thought of as having a psychological or sociological etiology are now being shown to have a physiological or biochemical basis as well. We now know that there are at least 8 factors that modify the functional state of the brain, thus affecting mood and behavior:

1. The individual genetic makeup.
2. The particular age of brain neuronal development which results in age-specific variability.
3. The functional plasticity of the brain during development, which contributes to the functional and structural shaping of the system.
4. The motivational state, affected by various biological drives, which channels behavior toward specific goals by setting priorities or prejudicing the context of particular types of incoming information.
5. The availability of memory-stored information and relating processing strategies.
6. The environment, which can adjust the incoming information depending on its momentary significance.
7. Disease or lesion of the brain, which could cause aberrant functional states.
8. Conditions of the metabolic/hormonal system of the internal biochemical environment of the CNS.1

Diagnostic Summary: According to the American Psychiatric Association, in its Diagnostic Statistical Manual of Mental Disorders (DSM-IV), depression is diagnosed according to eight primary criteria:

1. Poor appetite with weight loss, or increased appetite with weight gain.
2. Insomnia or hypersomnia.
3. Psychomotor agitation or retardation.
4. Loss of interest or pleasure in usual activities, or decrease in sexual drive.
5. Loss of energy and feelings of fatigue.
6. Feelings of worthlessness, self-reproach or inappropriate guilt.
7. Diminished ability to think of concentrate.
8. Recurrent thoughts of death or suicide.

If one has a total of five of these eight symptoms, one is defined as clinically depressed. This does not mean that if a patient has only four of these symptoms, the patient is not depressed. On the contrary, four of these symptoms would indicate a subclinical depression. Further, according to the DSM-IV the depressed state must be present for at least one month to be called depression. In many cases, depression is an appropriate reaction to a life event and specific medical treatment is not needed. In such cases, the patient may only require reassurance that the depression is not abnormal.

ETIOLOGY

Currently there are 4 basic theoretical models of depression:

1. The “aggression-turned-inward” construct. Though this model is apparent in many clinical cases, it has no substantial proof.
2. The “loss model.” This model postulates that depression is a reaction to the loss of a person, thing, status, self esteem, or even a habit pattern.
3. The “interpersonal relationship.” This approach utilizes behavioral concepts, such as the depressed uses their depression as a way of controlling other people. It can be an extension and outgrowth of such simple behavior as pouting, silence, or ignoring something or someone.
4. The “biogenic amine” hypothesis, which stresses biochemical derangements characterized by imbalances of neurotransmitters and other brain chemicals, such as serotonin and dopamine. Serotonin and dopamine are neurotransmitters, or chemicals in the brain which transmit information from nerve cell to nerve cell. These are the two neurotransmitters associated with depression, among other disorders.2

 

When the patient’s depression is thought to be best defined by one of the first 3 theories presented above, counseling should be the primary therapy. (These patients may also benefit from the nutritional therapy outlined at the end of this report.) However, the biogenic amine hypotheses has become the primary treatment approach used by physicians over the past several years. Many of the psychotropic drugs used by physicians are designed to correct or lessen suspected imbalances in the neurotransmitters of the brain. Despite the fact that there are many factors which are known to contribute to the depression, including nutrient deficiency or excess, drugs (prescription, illicit, alcohol, caffeine, nicotine, etc.), hypoglycemia, aspartame consumption, hormonal derangement, allergy, environmental factors, and microbial factors, most physicians’ first therapy of choice are the new anti-depression drugs. Anyone who has watched the news over the past 10 years has heard of incidences where someone taking one of these synthetic brain neurotransmitter altering drugs has experienced an adverse reaction. Perhaps the most notorious of these drugs is Prozac, manufactured by the Dista Pharmaceutical Corp. This drug is touted by its representatives as “safe and fast acting”. It gained national notoriety when several people who were being treated for clinical depression became aggressive and violent towards those around them.
The Physician’s Desk Reference, the exhaustive source for all prescription medications, documents the possible side effects of Prozac. Approximately 4% of patients taking Prozac during clinical trials developed severe skin rashes. Clinical findings associated with the rash included: fever, painful joints, carpal tunnel syndrome and respiratory distress. Vasculitis, or inflammation of the blood vessels, has developed due to Prozac use, and death secondary to vasculitis has been reported. Up to 15% of patients taking Prozac for depression report anxiety, increased nervousness and insomnia, plus abnormal dreams, agitation, decreased sex drive and abnormal ejaculations in men. Now, if you are seriously depressed and calling out for help, symptoms such as these cannot help your problem. They will only make your problems worse.
A second form of anti-depressant medications are the Monoamine Oxidase inhibitors (MAO), which are widely used in allopathic medicine. This medicine can have serious deleterious interactions with normal everyday foods. Elimination of foods containing the amino acid tyramine, which stimulates the release of norepinephrine, is mandatory or the patient could have a hypertensive crisis. Historically, foods necessarily excluded from the diet include cheese, chicken liver, sardines, red wine and alcoholic beverages and alcohol free beer and wine, dry sausage, avocado, cabbage, potato and banana.3 Patients who consume such products can suffer a hypertensive crisis, with blood pressure elevating into extremely dangerous levels.
Nutrient deficiencies have been shown to be a cause of depression. In fact, a deficiency in virtually any nutrient can result in depression. (Table 1 provides a list of the changes typically associated with specific vitamin deficiency states.4) The body has a remarkable way of conserving some nutrients that the body has in short supply. In these cases, we can measure the amount of a given nutrient or mineral and find if they are in an “acceptable level” in the body. However, for a given nutrient in a person, the level in the body may be sufficient not to produce gross symptoms of disease, however, the deficiency may be just at a level which can depress one’s mood. This can be related to Octane in a car’s gas tank. Regular gas has an octane rating of around 87, while premium has an octane rating of around 93. If we have a fine tuned race car which required premium gasoline, and continued to use regular, our car will continue to run, however, it will lose the performance we would wish for it to have. Our bodies were created to be fine tuned racecars. One of our problems is that instead of giving our bodies the premium fuel which has all the nutrients we need, we often give it fuel which is worse than the cheapest regular.
So, with the understanding that under the biologic amine hypothesis, nutrients which are factors utilized by the body to make neurotransmitters, nutrient deficiencies will cause depression in anyone. It is from this prospective that we will begin to show how several nutrients are utilized by the body to form the neurotransmitters in the brain, and specifically how deficiencies in any one of these nutrients can lead to depression and how supplementation has been medically and scientifically proven to relieve the symptoms of depression.

 

TABLE 1. BEHAVIORAL EFFECTS OF SOME VITAMIN DEFICIENCIES4

DEFICIENT VITAMIN BEHAVIORAL EFFECTS

Ascorbic Acid (Vitamin C) Lassitude, hypochondriasis, depression, hysteria

Biotin Depression, extreme lassitude, somnolence

Methylcobalamin (B12) Psychotic states, depression, irritability, confusion
memory loss, hallucinations, delusions, paranoia

Folic acid Forgetfulness, insomnia, apathy, irritability,
depression, psychosis, delirium, dementia

Niacin (B3) Apathy, anxiety, depression, hyperirritability,
Mania, memory deficits, delirium, organic
dementia, emotional lability

Pantothenic acid (B5) Restlessness, irritability, depression, fatigue
Pyridoxine (B6) Depression, irritability, hyperacousia (extreme
acute hearing)

Thiamine (B1) Psychosis, mental depression, apathy, anxiety,
irritability

Ascorbic Acid: We have all heard to take Vitamin C to prevent the common cold. But deficiencies are associated with states of depression. In a study of 885 psychiatric patients, the average plasma level of Vitamin C was 0.51 mg/100ml, compared to a level of 0.87/100 on 110 health non psychiatric patients.5 That is a 40% difference! Supplementation with Vitamin C has proven to relieve symptoms of some affective disorders, including depression. In a study reported by the British Journal of Psychiatry, 40 chronic male psychiatric patients randomly received either ascorbic acid (1 gram) or a placebo. After three weeks there was a significant decrease in the patients’ depression scale for those receiving the ascorbic acid, but there was no change for those receiving the placebo.6 Lancet also reported studies which demonstrated that many patients being treated for depression are deficient in vitamin C.7

Biotin: Biotin is one of the lesser known B vitamins. It is found in meats, dairy products and whole grain cereals, and its deficiency is associated with states of depression. In the Journal of Parenteral & Enteral Nutrition, researchers reported that patients receiving intravenous (IV) feedings developed a depression along with other symptoms including nausea, vomiting, insomnia, changes in their sensations of feel, headaches and lethargy. When supplementation of 300 micrograms of biotin was initiated, symptoms improved in only 5 days.8 The prestigious Journal of the American Medical Association reported a study in which patients were deprived of biotin to determine the effect on the body. After 10 weeks subjects began to report symptoms of depression, fatigue and changes in sensations of feeling. All symptoms were relieved by replacing biotin in the subjects’ diet.9

Tetrahydrobiopterin (BH4): This is a vitamin-like compound which functions as an essential co-enzyme in the formation of monoamines, or brain neurotransmitters. This substance is responsible for activating such enzymes as phenylalanine hydroxylase. This represents the first stage of neurotransmitter synthesis. Although BH4 is not a vitamin, patients with depression generally demonstrate low levels of this substance. It has been shown that these patients respond very favorably to supplementation. Unfortunately, specific BH4 supplements are not available in health food stores, however, BH4 synthesis is stimulated by folic acid, vitamin B12 and ascorbic acid.10,11,12,13

Folic Acid and Vitamin B12: Folic acid deficiency is the most common nutrient deficiency in the world, and depression is a common symptom of folate deficiency.14 In studies of psychiatric patients, as many as 30% have been shown to be deficient in folic acid and in one study, 67% of patients admitted to a psychogeriatric ward were folate deficient.15 In a study of 48 in-patients at a psychiatric hospital, it was found that the lower the patients serum folate levels, the more severe the patient’s depression.16 Furthermore, research has demonstrated that serum folate and B12 levels are low in a substantial proportion of patients suffering from various psychiatric syndromes, especially depression.17,18,19 As previously mentioned, folate is thought to stimulate BH4 formation and supplementation has been suggested for this reason.20,21,22,23 In a study reported in the Journal of Affective Disorders, it was shown that patients receiving folate had a significant reduction in their level of depression, as measured on the depression inventory.24 Patients with organic psychosis, endogenous depression and schizophrenia treated with folate fare much better than their matched controls. It has been suggested that correction of the deficiency may result in complete resolution of mental symptoms in some individuals.25 At the very least, folate supplementation has led to a considerable decrease in hospital stay when it has been utilized.26
The incidence of vitamin B12 deficiency in patients with psychiatric disorders is less than that of folic acid, however, serum B12 is a useful screening measure for older psychiatric patients. Vitamin B12 deficiency is most generally noted to be associated with a disorder in the blood called megaloblastic anemia. However, the megaloblastic anemia associated with B12 deficiency may not become apparent until long after serum levels have been greatly reduced. This means that symptoms of depression can occur long before vitamin B12 levels become clinically deficient.27,28,29,30
It has been demonstrated that folate and B12 are closely associated with the metabolism of a neurotransmitter, methionine. It has been observed that patients suffering from depression have decreased levels of a derivative of methionine, S-adenosylmethionine (SAM). SAM has been shown to possess antidepressant activity, comparable to tricyclic antidepressant medications when given to patients as a supplement.31,32,33,34,35,36

Riboflavin: A study reported in the British Journal of Psychiatry noted that of 172 successive psychiatric hospital admissions, riboflavin deficiency was associated with the diagnosis of depression.37 With this, reasonable supplementation is warranted.

Thiamine: When a patient is deficient in thiamine, or vitamin B1, the body’s metabolism will become acidic. With this acidity, brain chemistry will alter with decreased brain neurotransmitters which calm the system, and an increased neurotransmitters which stimulate the system.38 Severe thiamine deficiencies are often found in severe alcoholics, and results in diseases such as beri-beri and the Wernicke-Korsakoff syndrome. Researchers have demonstrated that thiamine restricted diets induce depression. In this study, 5 of 9 subjects became markedly depressed when thiamine was removed from their diets.39 Another study demonstrated that patients newly admitted to psychiatric hospitals generally have low levels of vitamin B1.40

Niacin: Niacin is an element which is utilized by the body in energy generation and metabolism. A niacin deficiency will result in a significant decrease in energy metabolism in the brain. Niacin supplementation could lead to a rise in tryptophan, an amino acid utilized in neurotransmission.41

Pyridoxine: Vitamin B6 is an important co-enzyme in the synthesis of all monoamines. Pyridoxine levels are typically quite low in depressed patients, especially those using oral contraceptives.42,43,44,45,46 Considering that pyridoxine is necessary for the conversion of tryptophan into serotonin, the neurotransmitter effected by many anti-depression medications, a deficiency in pyridoxine would lead to depression. Studies have shown that depressed patients with low pyridoxine status usually respond very well to supplementation.47,48,49,50 Improvement in tryptophan metabolism is generally the mechanism used to explain this effect, although pyridoxine is involoved in the synthesis and metabolism of all monoamines.51

Drug-Induced Depression

Often times, depression is a side effect of medicines prescribed by physicians. These medications include prescriptions such as corticosteroids and antihypertension medications. The incidence of drug induced depression is particularly true for drugs not generally thought of as medicines. Included in this category are: caffeine, oral contraceptives, and cigarettes. These drugs have been shown to change the normal balance of neurochemicals and neurotransmitters in the brain. It would be beyond our scope to examine every prescription which could cause depression, however, the number of people in the United States who are exposed daily to caffeine, cigarettes and oral contraceptives is staggering, and their implications in depression deserve a look.

Caffeine: Caffeine is the most widely used drug in our society. This is undoubtedly due largely to its ability to stimulate the system, its addictivity and the numerous and varied sources for its consumption. Caffeine is used in many consumer products that we are familiar with including beverages such as coffee, tea and colas. However, not so well known is the fact that caffeine is utilized in many over-the-counter drugs, such as some aspirin products, stimulants and analgesics.
The pharmacological effects of caffeine include increased brain and somatic (bodily) hormonal stimulation, stimulation of excitory brain nuerotransmitters and adrenal stimulation. When the adrenal glands are stimulated, as in the “fight or flight” response, sugar stored in the liver is released in mass quantities into the system. This is to provide energy to allow muscles to either fight or fly (run). Eventually this can lead to hypoglycemia, or low blood sugar. Caffeine also increases stomach acid secretion. Eventually this can lead to heartburn or gastritis. Caffeine will also inhibit sleep and promote diuresis, or frequent urination and dehydration.
It may be interesting to note that a typical 8 oz. cup of coffee contains between 50 and 150 mg of caffeine, depending upon what type of coffee is being consumed. A cup of tea contains around 50 mg, while a 12 ounce cola contains about 35 mg. The average American consumes 150-225 mg of caffeine per day, with the vast majority coming from coffee usage. Even though the average person consumes only 150-225 mg of caffeine a day, some people consume an excess of 7,500 mg per day. Excessive consumption of caffeine can produce severe symptoms similar to those found in generalized anxiety and panic disorders. Symptoms including depression, nervousness, heart palpitations, general irritability, recurrent headaches and muscle twitching have led to the coining of the term “caffeineism” to describe this clinical syndrome. As well, studies have shown that caffeine intake has been positively correlated with the degree of mental illness in psychiatric patients.52,53,54,55

Oral Contraceptives: Since their introduction, the use of oral contraceptives has been associated with inducing nutrient deficiencies. Of these deficiencies are folic acid, vitamin B12, riboflavin, pyridoxine, ascorbic acid, and zinc. As we have seen earlier, each of these nutrients is associated with depression in and of themselves. The decreased nutrients are normally metabolized by the liver, which suggests a decrease in hepatic (liver) metabolism. It is also interesting to note that levels of iron, copper, and vitamin A were generally increased.56
Oral contraceptives use different levels of the female hormone estrogen to “trick” the body into thinking it is pregnant when it is not. Estrogens have been shown to affect the mood of women taking the drug by competing for pyridoxal-5-phospate binding sites. Recall that pyridoxine is vitamin B6, which means that oral contraceptives actually make the pyridoxine in the woman’s body much less effective in doing its job. Oral contraceptives have also been shown to decrease glucose tolerance. It has also been shown that many of the side effects of oral contraceptive use can be corrected or reversed by vitamin B6 supplementation.57,58,59,60

Smoking: Ask any child and they will tell you that smoking is bad for the body. However, its implication in depression is not well known. Smokers have much higher levels of carbon monoxide than do non-smokers. A little explanation of blood gases is in order here. We breathe air which contains oxygen, O2. We breathe out carbon dioxide, CO2. In the lungs, oxygen binds to red blood cells, changing places on the blood cell with carbon dioxide. However, for some reason, the red blood cell prefers carbon monoxide over oxygen and when carbon monoxide binds to the red blood cell, it will never let go and will result in the death of the cell. So, when oxygen and carbon monoxide are in the lung at the same time, the carbon monoxide will bump the oxygen out of the way and bind the blood cell, while the oxygen is exhaled, not doing the body any good . What results is that there is less oxygen to run the body, fewer red blood cells to carry the available oxygen, both of which can make one listless, tired and depressed.
Nicotine, perhaps the most well known chemical smokers inhale, in itself actually causes a stimulation of brain waves. Nicotine also produces a significant rise in the concentrations of hormones associated with the flight or fight response, increasing blood pressure and pulse rate. Central to these effects is stimulation of adrenal hormone secretion, or adrenalin.61 The increase in these hormones actually decreases the brain’s synthesis of tryptophan. (Tryptophan is an amino acid which is later broken down to form serotonin. In the biogenic amine hypothesis, decreased serotonin is considered to be one of the causes of depression. In fact, serotonin is one of the neurotransmitters current anti-depression prescriptions seek to rise.) This is compounded by the fact that cigarette smoking is associated with increased sugar and caffeine consumption, as well as decreased levels of vitamin C.62,63,64

Hypoglycemia: The brain is only able to use glucose as an energy source, wheras muscles can use the breakdown products of fat for energy when glucose is scarce. When the levels of glucose in the blood fall, the body compensates by releasing the hormones of fight or flight. The liver stores large amounts of a form of stored glucose, called glycogen. One of the effects of these hormones is to dump the stored glucose from the liver into the blood stream to feed the muscles which are going to have to run or fight. One of these hormones, epinephrine, produces physical symptoms such as sweating, tremor, tachycardia, anxiety and hunger. When the onset of hypoglycemia is sudden, these hormonal symptoms will be clearly evident. If, however, the onset is gradual, these physical symptoms may not be recognized. Instead symptoms such as dizziness, headache, clouding of vision, blunted mental acuity, emotional instability, confusion and abnormal behavior predominate.65 There has been much controversy over the association of hypoglycemia and depression in America. Definitive research has yet to be completed. However, we do know two things. First, hypoglycemic patients report feelings of depression, lethargy, or lack of energy, and a host of other bodily complaints. It has also been demonstrated that psychiatric patients have a higher incidence of hypoglycemia than does the population at large.66,67,68

Aspartame: Aspartame is sold under the trade name NutraSweet or Equal. Despite FDA approval for this product, it is associated with a host of adverse effects, including depression, headache and memory loss. (Watch for a special EAT, DRINK AND BE HEALTHY report on aspartame in the very near future!)
Despite the reassuring claims the makers of NutraSweet provide, researchers Ralph Walton, M.D., Robert Hudak, Ph.D. and Ruth J. Green-Waite experienced a great deal of difficulty in their experiment on the safety of aspartame. Recently this research team conducted a research study of the problems associated with the ingestion of aspartame on people with mood disorders. Their study was admittedly small, including a total of 13 subjects, however the results were dramatic. All suffered from recurrent major depression. Five healthy hospital employees, including the hospital administrator, volunteered as the control group, or those who were given a placebo, for the study.
The results of the study were devastating. According to Dr. Walton the team’s research was halted after only 20 days by the Institutional Review Board of Western Reserve Care System, Youngstown, Ohio, because the reactions (including a detached retina and a conjunctival hemorrhage) among the patients with a history of depression were so severe they could not “ethically continue the study.” The research team concluded “individuals with mood disorders are particularly sensitive to this artificial sweetener (aspartame) and its use in this population should be discouraged.”69 Richard Wurtman, a pioneer in the study of nutrition and the brain, cautioned the FDA that, based on his extensive research, aspartame could significantly affect mood and behavior.70,71 Dr. Wurtman has demonstrated when aspartame is given to animals at levels comparable to those of people who drink a large amount of diet soda, the neurotransmitter levels in the brain which are known to fight depression are reduced significantly.72
Aspartame is composed of aspartic acid, phenylalanine and methanol. Methanol, also known as wood alcohol or paint thinner, is very toxic to the body. Its normal use is as an industrial cleaner or solvent. The amount of methanol in 1 gram of aspartame, or just one little blue packet of NutraSweet, is approximately 100 mg. To demonstrate just how toxic this can be, a child who consumes just 700 mg of aspartame would consume almost ten times the Environmental Protection Agency’s recommended daily limit of consumption for methanol.73
Don’t use diet sodas!

Environmental Factors

Many environmental factors can produce psychological symptoms of depression. Most notably of these are long term exposure to industrial solvents and heavy metals.74,75,76 Solvents, such as those used in paint and paint thinners, furniture repair, and boat building have been implicated in depressive and other emotional reactions. Hair mineral analysis, a process available through our office, is a proven, accurate and cost effective method of determining body levels of these toxins.77,78 Call our office at
1-800-726-1834 for details.

Candidiasis

The effects of candida on the body, particularly as it is related to fatigue and depression has become the focus of much attention. Candida has ben blamed for just about every symptom imaginable over the past decade, however, little actual research has been done to confirm patient reports. Researchers believe that candida may induce a variety of mental and neurological problems. It is not yet clear if these effects are due to intestinal overgrowth or byproducts of the metabolic process of the organism.78

Exercise: The value of an exercise program in the therapy of depression cannot be over-emphasized. The addition of exercise alone as a treatment regimen has proven to elevate mood and improve the patient’s ability to handle stress.80 Research has shown that increasing exercise and other physical activities is strongly associated with decreased symptoms of depression, anxiety and malaise (rundown feeling, insomnia).81

Recommended Treatment

 

Lifestyle: Adopt a regular exercise program, with at least 30 minutes of aerobic activity at least three times a week. We have prepared new exercise videos which are an excellent asset to your exercise routine. Also, eliminate smoking, oral contraceptives and caffeine.

Diet: Begin the diet program we presented for children suffering from Attention Deficit Disorder. This is available from our office by requesting the ADD supplement, Dec. 94. Aspartame must not be consumed in any form, and caffeine should be avoided. This report was included with your Eat, Drink and Be Healthy Program.

 

Supplements: In general, dependent upon individual needs, however we make the following recommendations
Cortico B ---2 capsules twice daily
Vitamin C---2000 mg two times daily.
Folic Acid---400 mg per day.
Sublingual B12---1 tablet daily
Magnesium---500 mg per day
Cod Liver Oil---2 Tbsp daily
Serenex---2 capsules twice daily
Ultimate Multiple---2 capsules twice daily

REMEMBER, if you are currently taking any medication, consult with your physician before eliminating or changing your usage!

REFERENCES:

 

1. Murray, M., N.D. and Pizzorano, J., N.D. Encyclopedia of Natural Medicine. Prima Publishing, Rocklin, CA 95677.
2. Krupp, M. and Chatton, M. Current Medical Diagnosis and Treatment, Chapter 17, Psychiatric Disorders, Lange Med Publ, Los Altos, CA, 1992.
3. Krause, M. and Mahan, L. Food, Nutrition and Diet Therapy, WB Saunders Co, Philadelphia, PA, 1984.
4. Krause, M. and Mahan, L. Food, Nutrition and Diet Therapy, WB Saunders Co, Philadelphia, PA. 1984.
5. Schorah, C.J., et al., Human Nutr: Clin Nutr, 37C: 447-52, 1983.
6. Milner, G., Ascorbic acid in chronic psychiatric patients: A controlled trial, Brit J Psychiat, 109:3+5+99, 1963.
7. Leitner, Z.A., Church, I.C., Nutritional studies in a mental hospital, Lancet, 1:565-67, 1956.
8. Levenson, J.L., J Parenteral & Enteral Nutr, 7(2):181-3, 1983.
9. Sydenstricker, V.P., et al., Observations on the ‘egg white’ injury in man, JAMA, 118:1199-1200, 1940.
10. Curtis, L., Neiderwieser, A., Levine, R., et al., Successful treatment of depression with Tetrahydrobiopterin, Lancet, 1:657-8, 1993.
11. Blair, J., Morar, C., Hamon, C., et al., Tetrahydrobiopterin in metabolism in depression, Lancet, 1:163, 1994.
12. Curtius, H., Muldner, H. and Neiderwieser, A., Tetrahydrobiopterin: Efficacy in endogenous depression and Parkinson’s disease, J Neural Trans, 55:301-8, 1992.
13. Leeming, R., Harpey, J., Brown, S. and Blair, J., Tetrahyudrofolate and hydroxycobolamin in the management of dihydroptridine reductase deficiency, J Met Def Res, 26:21-5, 1982.
14. Abou-Saleh, M.T., Coppen, A., The biology of folate in depression; implications for nutritional hypotheses of the psychoses, J Psychiat Res, 20(2):91-101, 1986.
15. Lipton, K., Mailman, R. and Numeroff, C., Vitamins: megavitamin therapy and the nervous system, In: Nutrition and the Brain, Vol. 3, Wurtman, R. and Wurtman, W. (eds.), Raven Press, New York, NY, 1979, pp. 183-264, Psychiat 1, 17:297-92, 1970.
16. Ghadirian, A.M., et al., Folic acid deficiency and depression, Psychosomatics, 21(11):926-9, 1980.
17. Reynolds, E., Preece, J., Baily, J. and Coppen, A., Folate deficiency in depressive illness, Br J Psychiat, 117:287-92, 1970.
18. Carney, M. and Sheffield, B., Associations of subnormal folate and B12 values and effects of replacement therapy, J Nerv Ment Dis, 150:404-12, 1970.
19. Zucker, D., Livingston, R., Nakra, R., Clayton, P., B12 deficiency and psychiatric disorders: A case report and literature review, Biol Psychiatry, 16:197-205, 1981.
20. Curtius, L., Neiderwieser, A., Levine, R., et al., Successful treatment of depression with tetrahydrobiopterin, Lancet, 1:657-8, 1993.
21. Blair, J., Morar, C., Hamon, C., et al., Tetrahydrobiopterin in metabolism in depression, Lancet, 1:163, 1994.
22. Curtius, H., Muldner, H. and Neiderwieser, A., Tetrahydropterin: Efficacy in endogenous depression and Parkinson’s disease, J Neural Trans, 55:301-8, 1992.
23. Leeming, R., Harpey, J., Brown, S. and Blair, J., Tetrahydrofolate and hydroxocobolamin in the management of dihydroptridine reductase deficiencies, J Ment Def Res, 26:21-5, 1982.
24. Coppen, A., Folic acid enhances lithium prophylaxia, J Affective Disord, 10:9-13, 1986.
25. Reynolds, E., Preece, J., Gaily, J. and Coppen, A., Folate deficiency in depressive illness, Br J Psychiat, 117:287-92, 1970.
26. Lipton, K., Mailman, R. and Numeroff, C., Vitamins: megavitamin therapy and the nervous system, In: Nutrition and the Brain, Vol. 3, Wurtman, R. and Wurtman, W.(eds.), Raven Press, New York, NY, 1979, pp. 183-264.
27. IBID
28. Reynolds, E., Preece, J., Baily, J. and Coppen, A., Folate deficiency in depressive illness, Br J Psychiat, 117:287-92, 1970.
29. Carney, M. and Sheffield, B., Associations of subnormal folate and B12 values and effects of replacement therapy, J Nerv Ment Dis, 150:404-12, 1970.
30. Zucker, D., Livingston, R., Nakra, R., Clayton, P., B12 deficiency and psychiatric disorders: A case report and literature review, Biol Psychiatry, 16:197-205, 1981.
31. Botz, M., Young, S. Bachevalier, J. and Gauthier, S., Effect of folic acid and vitamin B12 deficiencies on 5-hydroxyindoleacetic acid in human cerebrospinal fluid, Am Neurol, 12:479-84, 1982.
32. Reynolds, E. and Stramentinoil, G., Folic acid, S-adenosylethionine and affective disorder, Psychol Med, 13:705-10, 1983.
33. Reynolds, E., Carney, M. and Toone, B., Methylation and mood, Lancet, ii:196, 1983.
34. Bottiglieri, T., Laujndry, M., Martin, R., et al., S-adenosylmethionine influences monoamine metabolism, Lancet, ii:224, 1984.
35. Agnoli, A., Andreoli, V., Casachia, M. and Cerbo, R., Effects of S-adenosyl L-methionine (SAMe) upon depressive symptoms, J Psychiat Res, 13:43-54, 1976.
36. Caruso, I., Fumagalli, M., Boccassini, L., et al., Antidepressant activity of S-adenosylmethionine, Lancet, i:904, 1984.
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